Possible mechanism of captopril induced endothelium-dependent relaxation in isolated rabbit aorta

The mechanism of captopril, an angiotensin converting enzyme (ACE) inhibitor with sulfhydryl group (SH) in its structure, to produce an endothelium-dependent vasorelaxation was studied. In rabbit aorta with intact endothelium and precontracted with phenylephrine, captopril and superoxide dismutase (SOD) produced dose-dependent relaxation. Lisinopril, an ACE inhibitor without a -SH group in its structure, did not produce endothelium-dependent relaxation. It was observed that captopril, like SOD, produced the relaxation by protecting the EDRF from getting inactivated by superoxide anions as pyrogallol and methylene blue inhibited both the captopril and SOD-mediated relaxation. The free radical scavenging action of captopril is further substantiated by the observation that captopril, but not lisinopril, inhibited FeCl₃/ascorbic acid-induced lipid peroxidation in whole tissue homogenates of rabbit aorta to a level comparable to that of SOD. These results suggest that endothelium-dependent vasodilation produced by captopril may be due to its ability to scavenge superoxide anion and this property may be ascribed to the -SH group present in its structure.     

Chromatographic properties of the cadmium induced SOD isoform in Rhizopogon roseolus

Exposure of Rhizopogon roseolus mycelia to 15 mmol·dm⁻³ cadmium for 24 h induces a different pattern of Mn-SOD on polyacrylamide gels, probably being a changed form of an originally existing one. The presence of cadmium affects the chromatographic properties of this enzyme and its mobility through the acrylamide gel. This new isoform was purified using DEAE Trisacryl chromatography. Cadmium induced isoform adsorbed stronger to the ligands and was eluated with a Tris-HCl buffer containing 0.1 mol·dm⁻³ NaCl. SOD from control samples (not treated with cadmium) was eluated with the same buffer without NaCl.     

双歧杆菌抗衰老作用的初步研究

本文用双歧杆菌活菌液喂养老龄大白鼠,观察其血中抗衰老生化指标（ＳＯＤ、ＧＳＨ－Ｐｘ）和衰老生化指标（ＬＰＯ）的变化。试验组大鼠用双歧杆菌喂养两个月后,与对照组相比,前者血中ＳＯＤ活性显著升高（ｐ〈０．０１）,ＬＰＯ的含量显著低于对照组（ｐ〈０．０５）。采用自身对照,试验组大鼠用双歧杆菌喂养后与喂养前相比,ＳＯＤ活性显著升高（ｐ〈０．０１）,而ＬＰＯ的变化无显著性（ｐ〉０．０５）;对照组大鼠在试验期     

酸枣仁总皂甙对缺氧－再给氧心肌细胞的保护作用

按Laarse＇s方法建立培养心肌细胞缺氧-再给氧(A-R)模型,缺糖缺氧60min,再给氧30min.结果发现,缺氧组心肌细胞MDA含量增加,SOD活性降低,细胞膜脂质流动性下降,再给氧组上述改变加剧.酸枣仁总皂忒(ZS)能剂量依赖性地显著降低心肌细胞MDA含量,提高SOD活性,增加细胞膜脂质流动性,证明ZS有明显抗心肌细胞缺氧-再给氧损伤作用.     

Superoxide Dismutases and Anti-Oxidants Protected Mice from no-Reflow and Necrotic Damage Induced by Ischemia

A simple method in mice was established to screen anti-ischemic compounds. Thirteen times binding of rubber ring (1 × 1 mm, d = 42 mm) for 4.5 hrs, swelled the paws of 60% mice applied and 14 times binding swelled only of 5% mice. Critically reversible limit lay between these conditions. “All or none” rule dominated the paw swelling perhap due to different endogenous anti-oxidants' levels of individual mice. Determination of paw reversibility at 90 min of recirculation, was proved to be suitable. Swollen paws at this time returned normal and the paws with no-reflow dropped out by muscle necrosis after several days. Intravenous (i.v.) bovine Cu, Zn-SOD and bacterial Mn-SOD (3 - 10 × 10⁴ U/kg) or liposomal Cu, Zn-SOD (0.3 - 3 × 10⁴ U/kg) were protective (35-50%) by 14 times binding. Allopurinol (10-100 mg/kg) and D-mannitol (3-30mg/kg) was effective (25-55%). Catalase (i.v., up to 10⁵ U/kg) showed little protection, but local injection of 100 U/kg resulted in 50% protection. Glutathione (30 mg/kg) was suppressive only by local injection suggesting the importance of administration route. Desferal, heparin and nitric oxide synthesis inhibitor showed some protection, but indomethacin, mepyramine, ascorbate, vitamin E and dexamethasone were without effect. Excess dosing of all anti-oxidants tested, dramatically decreased their effects demanding caution for therapeutic trials.     

Superoxide dismutase does not inhibit the oxidation of cytochrome c and cytochrome oxidase.

An electrometric system was used to measure Ca⁺⁺ uptake by sarcoplasmic reticulum vesicles (SR). The method permits continuous recording of Ca⁺⁺ uptake and thus the valuation of kinetic parameters. Furthermore, the ultrasensitivity of the method permits to follow changes in Ca⁺⁺ concentration below 10^?6 M.     

Purification and properties of cytochrome P-450 from untreated monkey liver microsomes

Untreated monkey liver cytochrome P-450 (monkey P-450) has been purified to a specific content of 14.9 n mole/mg protein. The purified preparation was apparently homogeneous and the minimum molecular weight was estimated to be 50,000 by SDS-PAGE. Absolute spectrum of the oxidized form showed peaks at 565, 535 and 417 nm. The monkey P-450 was active in the mixed function oxidation of benzphetamine, aminopyrine, ethylmorphine, aniline and 7-ethoxycoumarin in the presence of rat liver NADPH-cytochrome P-450 reductase and DLPC. Anti monkey P-450 IgG could not inhibit rat P-450s (PB P-450, MC P-448(1) and MC P-448(2] catalyzed 7-ethoxycoumarin O-deethylation activities.     

Inhibition of replicon initiation by 12-O-tetradecanoylphorbol-13-acetate

To investigate the inhibition of DNA replication by tumor promoters, we incubated HeLa cells with 12-O-tetradecanoylphorbol-13-acetate (TPA; 10^?8 to 10^?5 g/ml) and quantified DNA synthesis on alkaline sucrose gradients. TPA was found to selectively inhibit replicon initiation without affecting DNA chain elongation in replicons that had already initiated. No inhibition of DNA synthesis was seen when cells were exposed to the nonpromoting derivative of TPA, 4-α-phorbol 12,13-didecanoate. Superoxide dismutase did not prevent the TPA-induced inhibition of initiation.     

Leukotriene B4, C4, D4 and E4 inactivation by hydroxyl radicals

Leukotriene B4 chemotactic activity and leukotriene C4, D4 and E4 slow reacting substance activity were rapidly decreased by hydroxyl radicals generated by two different iron-supplemented acetaldehyde-xanthine oxidase systems. At low Fe2+, leukotriene inactivation was inhibited by catalase, superoxide dismutase, mannitol and ethanol, suggesting involvement of hydroxyl radicals generated by the iron-catalyzed interaction of superoxide and H2O2 (Haber-Weiss reaction). Leukotriene inactivation increased at high Fe2+ concentrations, but was no longer inhibitable by superoxide dismutase, suggesting that inactivation resulted from a direct interaction between H2O2 and Fe2+ to form hydroxyl radicals (Fenton reaction). The inactivation of leukotrienes by hydroxyl radicals suggests that oxygen metabolites generated by phagocytes may play a role in modulating leukotriene activity.     

Estrogen regulation of superoxide dismutase in normal rat mammary tissues and mammary tumors

Multiple electrophoretic molecular variants of superoxide dismutase were demonstrated in normal rat mammary tissues and DMBA-induced rat mammary tumors. The specific activities of $\text{Cu}\text{Zu}$ superoxide dismutase in mammary tumors of estrogen-treated rats were not significantly different from those activities seen in normal rat mammary tissues. However, the enzyme activities of mammary tumors from untreated rats (no estrogen) were significantly lower than the activities of normal rat mammary tissues. Exogenous estrogen appeared to raise superoxide dismutase levels in DMBA-induced rat mammary tumors to those levels seen in normal rat mammary tissues.